Obesity Protocol

Why Insulin Makes People Hungry
One of the ways that excess insulin results in weight gain is that it causes people to be chronically hungry. A reason for this is that high insulin levels rapidly deplete glucose from the blood. This causes a state known as "reactive hypoglycemia," in which the blood becomes deficient in glucose because too much insulin is in the blood.

Low blood sugar-induced by hyperinsulinemia--produces a ravenous craving for glucose-producing foods. This hyperinsulin state promotes excess food intake and leads to a cycle where even greater amounts of insulin are produced to balance the increased calorie intake. The continuous consumption of glucose-producing foods leads to even more insulin secretion and contributes to the pathological accumulation of body fat.

Published studies show that even modest decreases in blood glucose concentrations are associated with hunger and the initiation of eating (Ludwig 2002). Indeed, insulin-induced hypoglycemia appears to provoke prolonged hunger, persisting long after restoration of normal blood glucose levels.

Furthermore, hyperinsulinemia (Kopf et al. 2001) and reactive hypoglycemia (Wursch et al. 1997) may preferentially stimulate consumption of high-glycemic index foods, leading to cycles of greater insulin secretion, followed by low blood sugar and the inevitable desire to rapidly consume more calories. Weight loss efforts (dieting) may exacerbate this phenomenon, as demonstrated by severe hypoglycemia after overweight subjects who were dieting consumed a high-glycemic index carbohydrate (Ludwig 2002). This helps to explain why so many diets fail, i.e., chronically high insulin levels cause people to crave the very carbohydrates that are making them fat. However, as you will learn later in this protocol, changing the type of food ingested is not a cure for obesity.

JAMA Study Indicates Hyperinsulinemia Causes Hunger
The anti-obesity potential of reducing serum insulin was reported in a study in the Journal of the American Medical Association (JAMA) that described the effects of serum insulin increase (hyperinsulinemia), hunger, and weight gain that ensues. The study concluded by stating: "It is possible that the hunger incident to hyperinsulinemia may be a cause of overeating, and therefore, the obesity that so often precedes diabetes" (Ludwig 2002).

Healthy people secrete enough insulin to efficiently metabolize glucose. Once enough glucose is taken up by the cells and removed from the blood, insulin then drops to very low levels in these metabolically balanced individuals. Overweight people, on the other hand, typically suffer from a metabolic disorder that results in elevated insulin secretion because the pancreas is attempting to overcome insulin insensitivity and drive excess glucose out of the blood.

There are serious misconceptions about why people accumulate so much body fat as they age. One overlooked factor is that overweight/obese people have startlingly high levels of insulin in their blood. When the blood is saturated with insulin, the body will not release significant fat stores, even when a person restricts their calorie intake and exercises.

Today's Diet Controversy
The role that excess insulin plays in inducing and maintaining obesity has not gone completely unnoticed. A number of popular weight loss books advocate dietary alterations that reduce or eliminate all high-glycemic food groups in order to suppress excess insulin secretion. Some of these diet programs go as far as to prohibit ingestion of healthy fruits.

Most obese individuals suffer from severe metabolic disorders that are not readily correctable by altering the amount or types of foods they consume. When we refer to the term "metabolic disorders," we are describing a host of pathological biochemical imbalances in an obese individual's body that precludes an individual from losing body fat. These same metabolic disorders also cause or contribute to the myriad of diseases associated with obesity. The information contained in this Obesity protocol explains how to correct the metabolic disorders responsible for inducing obesity and associated diseases.

The most compelling question confronting overweight Americans is: Why is no effective treatment available? Although scientific advances have been made in defining the metabolic mechanisms that occur in our bodies after we ingest calories, medicine has not progressed beyond the you-ate-too-much-so-you-got-fat concept.

The intrinsic difficulty with such simplistic explanations for weight gain is the fact that overeating does not automatically make a person become fat. We all know people with an unfair ability to eat anything and everything without gaining an ounce. There are published studies showing that dieting does not make an obese person thin over the long term (Toubro et al. 1998; Brand-Miller et al. 2002). Another study demonstrated no weight loss differences when obese individuals consume either high or low glycemic index diets (Astrup et al. 2002).

Blaming different types of food--or blaming the patient him/herself--may be popular, but it is monumentally unproductive. This attitude started in the early 1950s when scientists at the Rockefeller Foundation postulated that an increase in obesity that followed World War II was caused by excess protein consumption. Noting that 56% of the protein eaten enters the blood as glucose, they presumed this to be the source of excess sugar, which is easily stored as fat. However, restricting protein intake did not end the problem of obesity.

Caloric restriction "diets" and low carbohydrate diets have dominated for years because they do induce quick weight loss. Unfortunately, they do not cause significant fat loss. Too often, the weight that an obese person loses on a low carbohydrate diet not only comes back, but also will contain more fat than the weight lost through the painful diet.

One of the problems with modern diets is that they forget scientific principles that were long ago established relating to what happens when a person suddenly reduces their calorie intake. For example, if a person cuts calories from their normal diet, they initially lose a lot of protein, and its accompanying extracellular water, but almost no fat. The reason for the failure of diets to initially induce fat loss is that chronically high insulin levels preclude the release of fat from storage in the body. Since insulin blocks fat release, the body first burns up its protein reserves in response to dieting, which results in a quick reduction of body (protein) weight, but virtually no loss of body fat.

One early mathematical model showed that in response to cutting just 500 calories from one's daily diet, a weight loss of 620 grams (1.37 pounds) of protein tissue and water could occur as opposed to only 62 grams of body fat being lost (Albrick 1971). This model helps explain why people can easily lose total body weight when dieting, but fail to eliminate enough fat to resolve their obesity problem. When normal food intake is resumed, lost protein tissue is replaced with even more body fat. Taking into account these observations, Dr. Margaret Albrick, a prominent obesity researcher, concluded: ". . . available long-term studies show discouraging results on all diets. There is no basis for recommending any one diet over any other."

There are other metabolic adjustments that the body makes in response to lower food intake that can make it impossible to lose fat. People respond to a drop in food intake by immediately lowering production of the enzyme (5 -monodeiodinase) that converts the relatively inactive thyroxine to T3. It is the thyroid hormone T3 (triiodothyronine) that catalyzes the oxidation of glucose and its metabolites. Reduced levels of T3 cause onservation of calories, meaning that the body automatically burns fewer calories at rest. The minute a person cuts calories, whether from carbohydrate, fat, or protein, they turn down the rate at which calories are burned! (Braverman 1996). Overcoming a thyroid hormone (T3) deficiency will be discussed in more detail later in this protocol.

Cutting Calories/Carbohydrates Adds Fat!
Reduction in caloric intake causes a decrease in T3 levels (Merimee et al. 1976; Carlson et al. 1977; Palmblad et al. 1977; Vagenakis et al. 1977; Beer et al. 1989; Wadden et al. 1990), even when the decrease is caused by bypass surgery of gut (Wilcox 1977). The lowering of T3 is equal whether caused by lowering total calories or lowering carbohydrates (Spaulding et al. 1976; Azizi 1978). T3 is the calorigenic form of thyroid hormone. Lowering T3 automatically lowers the basal metabolic rate and favors conservation of energy--in other words, fat storage!

The Pathology of Obesity

Although many people experience life-long weight problems, many more find themselves beginning to gain weight as they age. The underlying metabolic disorder is the same, but the existence of the pathological factors involved in this condition is more easily understood in studying individuals who were thin in their youth. The primary difference between the two groups is not in the functional manifestations of the condition, but in its origin.

Elegant research involving sets of identical twins has confirmed beyond question the role of genetic predisposition in the etiology of life-long obesity (Hainer et al. 2001; Koeppen-Schomerus et al. 2001; Poulsen et al. 2001; Kunesova et al. 2002a,b). If one of two parents is obese, the chances of their offspring developing obesity are 4 in 10 (40%). If both parents were overweight all their lives, the chances jump to 80% that the offspring will also be overweight. However, the metabolic changes that cause weight gain are virtually the same in both inherited and acquired obesity. Correction of these functional changes will result in normalization of weight whether the obesity is inherited or a consequence of aging.

Those who start out life being slim enjoy the seemingly unfair ability to eat as much as they want of whatever they want without ever gaining weight. They rarely pay any attention to their diets and take for granted that their clothing will always fit.

Most individuals begin a steady march into obesity during their late twenties. It is in the late twenties that most people begin to lose muscle mass--unless they work hard to retain it. Between the ages of 26 and 28 that loss of muscle mass can represent from 3-10% of lean tissue. Some are lucky enough to not see an increase in body fat replacing the lost muscle for 5 or so years. Those who are athletic may not notice that their slim days are behind them for 10 or 12 more years. However, by age 39 the vast majority of Americans are forced to face the fact that they are overweight.

The normal changes of aging that make it easy for people to gain weight include alterations in endocrine hormone levels. Unfortunately, insulin, cortisol, and estrogen (in men)--hormones that do not decrease as we grow older--favor fat gain. Later in the protocol, you will learn how each of these hormones plays a role in causing people to add fat and what can be done to restore a more youthful hormone balance that promotes calorie wasting rather than fat storage.

The Insulin Trap
Prior to the 1950s, scientists believed that stored fat was relatively inert and that once adipose (body fat) tissue was formed, very little metabolic activity took place in fat cells; however, it was then learned that the triglyceride stores of fat tissue are constantly turning over (Bjorntorp 1996). An enzyme called lipoprotein lipase controls the passage of fat precursors into the fat cell. The breakdown of stored fat and the passage of these breakdown products out of the fat cell are controlled by a different enzyme, hormone sensitive lipase. Insulin prevents the action of the second enzyme (hormone sensitive lipase).

As long as insulin is present in the blood, stored fat cannot be mobilized--it is locked into the cell. The bad news is that fasting insulin levels are elevated in obesity (Kolterman et al. 1980). In normal health, when glucose in blood drops below 83 mg/deciliter, insulin vanishes. When an individual is overweight, insulin never vanishes.

Insulin not only keeps fat in storage, but insulin also stimulates the production of new fat. It even lowers levels of the amino acid carnitine in the liver. Carnitine is needed to carry fat precursors into the mitochondria, where the fat precursors can be burned as heat to "waste" calories.

Overweight individuals have long been known to have high fasting insulin levels--in fact, Dr. Margaret Albrick observed that elevated fasting insulin is the critical difference between thin and obese persons (Albrick 1971).

As the undeniable role of insulin in causing and maintaining obesity has come to the attention of popular "diet" and "weight-loss" experts, many useless solutions have been suggested. The many attempts to lower fasting insulin by dietary restriction, either of carbohydrates or of high glycemic foods, arose from the observation that elevation in blood glucose is a primary stimulus of insulin release. However, it is not the only such stimulus. Amino acids such as L-leucine have a strong effect on insulin release, as do many digestive hormones (Galabova et al. 1976; Malaisse et al. 1984; Giroix et al. 1999).

The early demonstration that glucose given orally produces a much greater insulin surge than the same amount of glucose given intravenously proved that elevation of blood glucose alone is not the source of hyperinsulinemia (Mclntyre 1978). This enhanced release of insulin is thought to be caused by gut hormones. No diet is effective in correcting fasting hyperinsulinemia in obese individuals.

Obesity and metabolic diabetes (in the early stages) are also associated with an increase in the mass of the tissue that produces insulin, the beta cells of the islets of Langerhans (Mclntyre 1978). Both high-carbohydrate and high-protein diets have the same stimulatory effect on increased islet cell mass.

As long as insulin is present in the blood, fat cannot be released from storage. Thus, the weight lost by overweight people in response to "dieting" is largely protein and water. "Dieting" or lowering food intake can be seen to have two disastrous effects on obesity:

Lowering of metabolic rate by turning down conversion of T4 to T3
Depletion of lean tissue
Exercise, the other popularly prescribed "treatment" modality, has only one disastrous consequence for obese individuals: exercise lowers the need for insulin (Kirwan et al. 2002; Reynolds et al. 2002). Obese individuals already have too much insulin. Therefore, exercise causes the excess to be that much more excessive!

Please note that all these statements refer to persons who are overweight. Caloric restriction and exercise are beneficial for individuals who are thin.

Initial Treatment for Obesity

Although fasting hyperinsulinemia cannot be adequately corrected by diet alone, it must be brought under control before an individual can start to lose body fat. Therefore, the first step in effective treatment of obesity is lowering fasting insulin levels. (After years of experimentation, a nutritional supplement based on standardized extract of avocado has been shown to lower fasting insulin levels in overweight and obese human test subjects. Avocado extract will be discussed in more detail later in the protocol.)

Although what an individual eats may not have a critical influence on weight gain, when an individual eats most certainly does (Taylor et al.1999). Early observations had also indicated that the majority of obese people take in most of their daily calories in a relatively short period in the evening (Dole et al. 1953; Stunkard et al. 1955, Hollifield et al. 1964). Based on these observations, a first step in treating obesity is changing the time of day when most calories are consumed. By shifting consumption of high-calorie foods from late in the day to earlier in the day, there is great potential that some of the fundamental metabolic disorders (disruptions in glucose, insulin, and leptin metabolism) that prevent obese people from losing body fat can be corrected (Taylor et al. 1999).

In clinical weight loss practice, overweight and obese patients were told to alter the time of day when they consumed their food and to consume standardized avocado extract tablets in the evening to suppress food cravings. The result was rapid and sustained fat loss in those who adhered to the following instructions:

Immediately after awakening, eat a large breakfast. If you want a banana split, eat it at breakfast! Eat as much as you want of whatever you want. The reason we advocate a liberal breakfast is that you should follow this program for the rest of your life. If you are continuously deprived of the foods you like, at some point you might rebel and begin eating at the wrong time of the day. Ideally, breakfast will consist of fresh fruit and whole grains, but if you need to consume high calorie foods or prefer to do so, do so in the morning and not late in the day.
Late in the morning, have a snack equivalent in calories to a hamburger and potato fries. Healthier foods are recommended, but for the purposes of complying with this program, eat whatever you want at this time of the day instead of waiting until the evening when these calories readily convert to body fat.
Mid-afternoon, have another snack equivalent to the calories obtained from a tuna salad sandwich on whole wheat bread and some fruit.
No later than 6:30 p.m., have a modest dinner such as fish or lean chicken, potato, and several vegetable servings.
After dinner, consume nothing by mouth but standardized avocado extract pills and the water required for swallowing them!
Two avocado extract pills may be taken if hunger returns later in the evening.
The objective of this protocol is to reduce fasting insulin to zero or near zero levels. That is why it is critical that no food be consumed after 6:30 p.m. This program is designed to achieve a critical purpose, i.e., to normalize fasting insulin so that body fat can be released from storage.

It may take a week for some obese individuals to wake up hungry (as they are supposed to do) and not have the desire to eat after 6:30 p.m. After 45 days of following this program that alters the time of day when calories are consumed, an improvement in several metabolic parameters should become evident, including a reduction in fasting insulin levels. Enough fat loss should have occurred during this initial 45-day period to motivate an individual to reduce total calorie intake and begin to exercise. Using standardized avocado extract pills makes restricting calorie intake much easier by reducing carbohydrate cravings.

Following this six-step program described has resulted in many overweight patients achieving a normal weight in a relatively short time period. Most obese individuals experienced sustained reductions in body fat, especially in the abdominal area. Some patients did require additional therapies to correct underlying metabolic disorders responsible for their inability to lose body fat. These supplementary therapies will be discussed later in the protocol, but first the beneficial mechanisms that occur when the calorie burden is shifted to early day eating will be explained.

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These statements have not been evaluated by the FDA. These products are not intended to diagnose, treat, cure, or prevent any disease